Need to know - cardiac arrhythmias
Cardiologists Professor John Camm and Dr Malini Govindan answer GP Dr Mandy Fry’s questions on rate versus rhythm control and ‘pill in the pocket’ regimes
Cardiologists Professor John Camm and Dr Malini Govindan answer GP Dr Mandy Fry's questions on rate versus rhythm control and ‘pill in the pocket' regimes
1. What factors influence whether we should be aiming for rate or rhythm control in patients with AF? What factors determine whether DC cardioversion is indicated?
A rhythm control approach is usually preferred for patients who are relatively young, active and symptomatic.
DC cardioversion is considered in patients with:
• new onset AF
• lone AF or
• AF of short duration, usually less than one year.
It is also considered in those who are symptomatic with palpitations, chest pain and dyspnoea even after controlling the heart rate with medication.
DC cardioversion is also used only in patients without significant structural heart disease or where the cause of the AF has either been treated, is transient or is relatively mild. Patients with significant underlying heart disease or other disease that may provoke recurrence of AF are usually not selected for cardioversion.
Rate control is offered to subjects with chronic heart disease and damage to the heart including moderate to severe left atrial dilatation or left ventricular systolic dysfunction. It is also considered for elderly patients with a sedentary lifestyle and for those in whom cardioversion has failed despite several attempts.
2. Which patients benefit from implantable cardiac defibrillators? Do they need to take any special precautions?
Indications for ICD implantation have evolved considerably over the past decade – go to the online version of this article on pulsetoday.co.uk/clinical for a full table of current indications.
Research has clearly established that ICDs improve survival compared with anti-arrhythmic drugs for secondary prevention of sudden cardiac death and they have been recommended by the American Heart Association, the American College of Cardiology and the European Society of Cardiology.
Large trials have also shown ICDs to be effective for the primary prevention of sudden death. They improve survival in selected patient groups who have not previously had a cardiac arrest or life-threatening ventricular arrhythmia.
Some individuals who are resuscitated from cardiac arrest may have a reversible cause, such as myocardial ischaemia. In such patients, coronary revascularisation is required to reduce the risk of sudden death and an individual decision on ICD implantation may be required.
3. Do patients with a permanent pacemaker need monitoring in primary care? How long does the battery last? Does the patient get any warning of a low battery or do you always replace it before that can occur? How careful do patients need to be in avoiding electronic barriers such as those in libraries and airports?
Patients with pacemakers generally have their devices monitored by a cardiologist or at a hospital-based pacemaker clinic. On initial implantation patients are reviewed at one month but thereafter on a six- or 12-month basis.
Battery status is regularly checked at these follow-up sessions and the pacemaker is replaced before the battery is depleted. Battery life depends on how much the pacemaker is triggered.
The patient does not get any warning of pacemaker battery rundown. Generally the battery will last at least seven years.
Nor regular monitoring of a pacemaker is needed in primary care. But if there are complaints of dizziness, syncope, palpitations or, in the case of defibrillators, frequent shocks delivered from the device, the patient should be referred to a cardiologist to investigate device malfunction or lead displacement.
Interference with pacemaker function by anti-theft devices is uncommon if the patient simply walks through the electromagnetic field emitted by these devices. However, if the patient stands within the field the pacemaker may pick up signals that it interprets as spontaneous heartbeats and because modern pacemakers work on demand they may stop stimulating the heart until the patient walks on or collapses.
4. What is the ‘pill in the pocket' regimen? Which patients is it suitable for? Would they still benefit from anti-coagulation?
The pill-in-the-pocket approach involves the patient taking anti-arrhythmic medication only when an episode occurs rather than regularly as prophylaxis.
This approach is generally used in selected patients with paroxysmal AF or supraventricular tachycardia (SVT) who have infrequent symptoms.
The main concern with this approach is the risk of ventricular proarrhythmia associated with some anti-arrhythmic drugs. Usually an inpatient or A&E trial of these drugs – with cardiac monitoring – must be carried out before they can be used safely at home.
The drugs that have been studied for use in AF are:
• Class Ic – membrane stabilising drugs – flecainide and propafenone
• Class III – amiodarone for AF
• Class IV – calcium channel blockers - verapamil for SVT.
Patients who may be suitable for a ‘pill-in-the-pocket' method of treatment are listed in the box below.
Anticoagulation is needed irrespective of the treatment given for AF and is based on the risk of stroke.
The algorithm mostly used to assess stroke risk in AF is the CHADS score (Congestive heart failure, Hypertension, Age over 75, Diabetes, Stroke). One point is allocated for all risk factors except stroke, which receives two points. If patients have a CHADS score of more than 1, they should be anti-coagulated with warfarin. If the CHADS score is 1, then either aspirin or warfarin could be given and for those whose CHADS score is 0, aspirin alone is adequate.
5. Some patients who undergo DC cardioversion also seem to be treated with anti-arrhythmic drugs such as amiodarone or sotalol. What is the rationale behind this? How long do we need to prescribe these drugs for?
DC cardioversion isn't always successful in restoring and maintaining sinus rhythm.
In some cases, there is no conversion and in other cases AF recurs within minutes (early recurrence) or within days to weeks (subacute recurrence). Recurrence beyond two weeks is considered late recurrence.
The use of concomitant anti-arrhythmic medication increases the chance of successful cardioversion and maintenance of sinus rhythm. After evaluation of several trials assessing concomitant use of anti-arrhythmic drugs pre- and post- cardioversion, NICE guidelines recommend that the use of amiodarone, sotalol, flecainide and possibly propafenone increase the chance of successful cardioversion in comparison with controls and reduce AF recurrence post- cardioversion. These medications are generally reserved for patients with a perceived increased chance of unsuccessful cardioversion and should be given four weeks before cardioversion and continued for at least one year. Anti-arrhythmic drugs should never be discontinued without consultation with a cardiologist.
6. We're all familiar with AF being an indication for anticoagulation. But do other arrhythmias carry a similar increased risk of cardiovascular events?
The role of anticoagulant therapy for AF is based on prospective randomised trial data but no such data are available for atrial flutter. However, observational studies have shown that the risk of embolisation in atrial flutter ranges from 1.7 to 7%.
Studies have also shown that the incidence of atrial thrombus is up to 30% in patients with atrial flutter who are not anticoagulated. Furthermore, atrial stunning – the transient depression of atrial mechanical function – after conversion of atrial flutter seems to persist for several weeks. So the risk of developing an embolic event is similar to AF.
The consensus from the AHA/ACC/ESC is that the guidelines for anticoagulation in patients with AF should extend to patients with atrial flutter. If patients with isolated atrial flutter – and no associated AF – undergo catheter ablation, anticoagulation can be stopped in successful cases.
SVTs such as atrioventricular nodal re-entrant tachycardia (AVNRT) and atrioventricular re-entrant tachycardia do not carry this risk of systemic embolisation as atrial contraction is unimpaired.
7. In patients presenting with palpitations we tend to routinely measure their TFTs, U&Es and calcium. How commonly do such biochemical disturbances result in arrhythmias? Are there any other investigations we should be considering?
Endocrine and biochemical disorders can induce ventricular arrhythmias and sudden cardiac death by excess or insufficient levels of hormones or electrolytes – for example phaeochromocytoma, hyperthyroidism or hypothyroidism.
The hormone excess can result in tachycardias, which may progress to atrial or ventricular arrhythmias. They can also cause changes in the myocardium – for example in acromegaly – or biochemical imbalances such as hyperkalaemia in Addison's and hypokalaemia in Conn's syndrome.
Endocrine disorders can also accelerate the progression of other conditions such as hypertension and dyslipidaemia which promote coronary artery disease, predisposing to increased risk of ventricular arrhythmias.
A routine biochemical and endocrine screen for a patient with new palpitations should include electrolytes – calcium, potassium, sodium – and TFTs. Baseline blood pressure should also be recorded.
8 Many of the drugs we seem to commonly prescribe have the potential side-effect of lengthening the QT interval. How significant is this in clinical practice? Are there groups of patients with whom we should be particularly cautious?
It is well recognised that a prolonged QT interval (congenital or acquired) on the surface ECG is associated with increased risk of Torsade de pointes (TdP) and sudden death. The blockade of the outward potassium current is responsible for this pro-arrhythmic effect. Measurement of the QT interval must be corrected for heart rate.
The most common cause of an acquired long QT syndrome is drug treatment, with anti-arrhythmics being commonly implicated. However, several non-cardiac drugs have been found to cause QT prolongation or TdP including
• non-sedating antihistamines
• macrolide antibiotics
• tricyclic antidepressants
In the UK, non-cardiac drugs with pro-arrhythmic potential – those with an official warning of QT prolongation or TdP – represented 3% of total prescriptions. Therefore, the risk of drug-induced arrhythmias is serious.
The list of drugs with a propensity to cause QT prolongation is growing and has attracted significant regulatory attention – see table below.
Physicians and pharmacists who prescribe these drugs must be aware of these risks, taking appropriate precautions. A useful website is here.
These drugs should be avoided or be prescribed with caution in patients with risk factors for TdP (see table below) and those with structural heart disease. Regular ECG monitoring and assessment of blood potassium levels may be needed (see BNF for further advice). Co-administration of multiple drugs, especially other QT-prolonging drugs and, where appropriate, drugs that inhibit metabolism, such as cytochrome P450 inhibitors, must be avoided.
9. Is it true that, in the absence of structural heart disease, the use of an anti-arrhythmic to suppress ventricular arrhythmias actually increases mortality? Should we therefore just be reassuring patients with infrequent symptoms or will they still benefit from review by a cardiologist?
The appropriate management of ventricular arrhythmias including premature ventricular contractions (PVCs) , non-sustained ventricular tachycardia (NSVT) and sustained monomorphic or polymorphic ?ventricular tachycardia? (VT) depends on an appreciation of the mechanism of the arrhythmia, possible associated medical conditions and exacerbating factors. With the exception of ß-blockers and possibly amiodarone, anti-arrhythmic drugs have not been shown to be effective in the primary management of ventricular arrhythmias or in the prevention of sudden cardiac death. It may be used as an adjunctive therapy in some patients under certain circumstances such as LV dysfunction.
Class IA (quinidine, procainamide, disopyramide) and class III (sotalol, amiodarone, dofetalide) Anti-arrhythmic drugs (AADs) prolong repolarisation and cardiac refractoriness and can result in deleterious side-effects. This results in prolongation of the QT interval on the surface ECG (generally >450ms) and may be pro-arrhythmic in 2-4% of patients. This inhomogenous prolongation of repolarisation renders the myocardium vulnerable to inappropriate re-entry currents, which may trigger and then sustain ventricular arrhythmias and can lead to VF or even death.
The most important of these arrhythmias is TdP which predominantly occurs with Class 1A and Class III drugs and may cause a life-threatening polymorphic VT. The risk of TdP precludes the use of Class 1A and Class III AADs in high-risk patients (see table 2)
Single or infrequent PVCs in the absence of structural heart disease are not of prognostic significance and patients can be managed with reassurance or if symptomatic, ß-blockers. Occasionally highly symptomatic PVCs can be treated with ablation of the focus from which the ectopic beats arise. Patients with repetitive forms of ectopy, sustained ventricular arrhythmias or polymorphic ventricular tachycardia warrant referral to a cardiologist for further evaluation.
10. We often seem to get back 24-hour ECG results with runs of trigeminy or bigeminy, which rarely seem to correlate with the patient's symptoms. Are these of any significance?
The significance of single or repetitive forms of PVCs depends on the degree of symptoms and the presence or absence of structural heart disease.
In those without structural heart disease, PVCs have no mortality risk implications. In contrast to PVCs and monomorphic patterns of NSVT, polymorphic ventricular tachycardia, in the absence of structural heart disease is associated with risk. Such subjects often have abnormalities at a molecular level or electrolyte or drug related effects.
A community-wide epidemiology study in Michigan found that PVCs in subjects under 30 with structurally normal hearts had no prognostic significance but began to influence risk in those over 30.
In contrast, while PVCs at rest are regarded as low risk, PVCs elicited during exercise or during the recovery phase correlate with increased mortality risk and a greater burden of recovery-phase arrhythmias. ß-blockers can be used to suppress PVCs if patients are symptomatic. Anti-arrhythmic drugs have not been proven to offer benefit in such patients.
If the burden of ectopy is high (>100/hour) or there are frequent and complex ectopy patterns (bigeminy/trigeminy) or reports of sustained arrhythmia, a search for structural heart disease should be made.
These patients should be evaluated with an echocardiogram and in some instances with invasive angiography or MRI.
When the PVCs have a left bundle branch block–like shape (positive in V1 and late negative waves in V6), the diagnosis of arrhythmogenic right ventricular cardiomyopathy should be considered
Exercise stress testing is used to evaluate arrhythmias related to ischaemia or to rate related/catecholamine dependent arrhythmias such as to assess for right ventricular outflow tract tachycardia.
PVCs and runs of NSVT in the presence of structural heart disease do contribute to an increased mortality risk, the magnitude of which depends on the extent of the heart disease. In patients with a history of MI, frequent and repetitive forms of ventricular ectopic activity in the presence of reduced left ventricular systolic function are associated with an increased risk of sudden cardiac death during follow-up. Most studies quote a frequency of 10 PVCs per hour or repetitive complex forms of ectopy as thresholds for increased risk.
Ventricular arrhythmias during exercise or ambulatory recording do not have additive predictive value of risk – risk is already high because of underlying heart disease. Suppression of ventricular arrhythmias with anti-arrhythmic drugs as a therapeutic target to prevent sudden cardiac death has not been shown to offer mortality benefit in this sub-group.
Dr Malini Govindan is a specialist registrar and British Heart Foundation research fellow at St George's Hospital, London
Competing interests None declared
Professor A John Camm is BHF professor of clinical cardiology at St George's, University
Competing interests None declaredRegular ECG monitoring may be needed in patients taking QT prolonging drugs Regular ECG monitoring may be needed in patients taking QT prolonging drugs What I will do now What I will do now
Dr Fry responds to the answers to her questions
• I will refer patients who have good insight and infrequent occurrences of AF or SVT for consideration of the ‘pill-in-the-pocket' regimen.
• It is useful to get clarification over the need for anticoagulation in ‘pill-in-the-pocket patients.
• In patients who have been successfully cardioverted I will discuss the possibility of discontinuing their
anti-arrhythmic drugs with the cardiologists after a year.
• It is interesting to note similar rates of embolism formation in AF and atrial flutter.
• I will consider the use of anticoagulation in patients with atrial flutter.
• I will measure calcium levels (as well as U&Es and TFTs) in patients presenting with new palpitations
• I will be more cautious in prescribing drugs that have the potential to prolong the QT interval.
• I will be especially cautious with patients taking multiple medications.
• I will reassure my patients with pacemakers that they can continue to use the library but that they shouldn't loiter near the anti-theft devices.
Dr Mandy Fry is a GP in Cirencester, Gloucestershire, and senior primary care lecturer at Oxford Brookes University